2. The word "vitamin" comes from the Latin word vita,
means "life".
Vitamins are chemicals found in very small amounts in
many different foods.
“vitamins have been defined as organic compounds
which are required in minute amounts to maintain
normal health of organisms’.
2
4. A Short History
From about 1500 BC it was of Vitamins
known that various diseases
could be treated with specific
foods.
. In 1880 Christian Eijkman
dutch physician and professor
of physiology
produced vitamin-deficiency
conditions in animals on an
experimental basis and
then reversed the condition
with an appropriate feeding
regimen.
4
5. Frederick Hopkins, English biochemist said in 1906 that
foods contain a small amount of "growth factors" needed to
sustain growth and life itself.
The general category of "vitamins" was defined as (1)
substances found to be absolutely necessary for life (i.e., vital)
and which (2) the body cannot synthesize on its own.
5
6. In 1912 Kaziemirz funk Polish-British-American
biochemist named these growth factors “vitamines”
vit + amine
Funk's original term "vitamine" was changed to "vitamin"
when many scientists identified, purified, and synthesized all
of the vitamins and discovered they did not all contain
nitrogen.
6
7. In the 1930s a scientific discovery demonstrated the
biochemical functions of the vitamins and established the
body's requirements for them. From then on, they have been
commercially produced.
7
9. Fat soluble Vitamins
They are soluble in fat.
Bile salts are essential for there absorption.
They are generally stored in liver.
They are not excreted in urine.
9
10. Vitamin A
It is recorded in the history that Hippocrates(about
500 B.C.) cured night blindness.
He prescribed to the patients ox liver (in
honey),which is now known to contain high quantity
of vitamin A.
10
11. VITAMIN A :- Is widely distributed in animal and plant
foods
animals –pre-formed – Retinol.
plants – pro-formed - carotene
11
13. Retinal (vitamin A aldehyde) :
This is an aldehyde form obtained by the oxidation of
retinol.
Retinal and retinol are interconvertible.
13
14. Retinoic acid (vitamin A acid) :
produced by the oxidation of retinal.
However,retinoic acid cannot give rise to the formation
of retinal or retinol.
14
15. Beta-Carotene (provitamin A) :
Found in plant foods.
lt is cleaved in the intestine to produce two moles of
retinal.
ln humans, this conversion is inefficient, hence beta-
carotene possesses about one-sixth vitamin A activity
compared to that of retinol.
15
16. Dietary Sources of Vitamin A
Plant sources Animal sources
Sweet potatoes Chicken liver
Carrots Cod liver oil
Pumpkin Fish oil
Winter squash Canned beef stew
Cantaloupe Eggs
Pink Grapefruit Fish
Mangoes Shellfish
Apricots Butter
Oranges Fortified margarine
Spinach Cheese
Kale Whole milk
Beet greens Fortified skim milk
Broccoli Fortified low fat dairy
Dark green leafy products
vegetables 16
17. DAILY REQUIRMENT
Men and women – 600 mcg.
Pregnancy and lactation – 950 mcg.
Infants – 350mcg.
Children – 600mcg.
17
18. ABSORPTION & STORAGE
The liver has enoromous capacity
to store – in the form of retinol
palmitate.
Free retinol is highly active but
toxic & therefore transported in
blood stream in combination with
retinol binding protein (liver)
18
19.
20. Physiological Functions of Vitamin A
Vision
Epithelial cell
"integrity’
Reproduction
Resistance to
infectious disease
Bone remodeling
Growth
20
21. Vision
Retinal is a necessary
structural component of
rhodopsin , the light
sensitive pigment within
rod and cone cells of the
retina.
Rods are involved in
dim light vision
Cones are responsible
for bright light &
colour vision
21
24. colour vision
The colour vision is governed by colour sensitive
pigments porphyropsin (red), iodopsin
(green) and cyanopsin (blue).
All these pigments are retinalopsin
complexes.
When bright light strikes the retina, one or more of
these pigments are bleached,depending on the
particular colour of light.
The pigments dissociate to all-trans-retinal and opsin.
And this reaction passes on a nerve impulse to brain 24
25. Epithelial cell "integrity
Many epithelial cells appear to require vitamin A for
proper differentiation and maintenance.
Lack of vitamin A leads to dysfunction of many epithelia
The skin becomes keratinized and scaly, and mucus secretion
is suppressed
25
26. Reproduction:
Normal levels of vitamin A is required for sperm production,
Normal reproductive cycles in females require adequate
availability of vitamin A.
Bone remodeling:
Normal functioning of osteoblasts and osteoclasts is dependent
upon vitamin A.
26
27. Resistance to infectious disease
vitamin A deficiency has been shown to increase the frequency
and severity of disease.
Several large trials with malnourished children have
demonstrated dramatic reductions in mortality from diseases
such as measles by the simple and inexpensive procedure of
providing vitamin A supplementation.
27
30. Deficiency of Vitamin A
Most susceptible
populations:
Preschool children with
decreased intake
Poor persons
Older adults
Alcoholism
Liver disease (limits
storage)
Fat malabsorption
31. The signs of vitamin A deficiency
Ocular
Extra ocular
Night blindness.
Retarded growth
Conjunctival xerosis
Skin disorders
bitot’s spot
Effect on reproductive
Corneal xerosis
organs.
keratomalacia
Effect on bone
31
33. Night blindness
Lack of vitamin A
causes night blindness
or inability to see in
dim light as a result of
inadequate pigment in
the retina.
Earliest symptom
33
34. Conjunctival xerosis
Conjunctiva becomes dry, lustureless and non wettable.
Described as “emerging like sand banks at receding tide”
Commonly involves the interpalpebral area of temporal
quadrants
Advanced cases > entire bulbar
conjunctiva involved
Conjunctival thickening,
wrinkling & pigmentation.
34
35. Bitot's spots
Raised, silvery white,
foamy, triangular patch of
keratinised epithelium.
Usually bilateral and
temporal aspect.
35
36. Corneal xerosis
Earliest change is
punctate keratopathy
followed by haziness
and/or granular pebbly
dryness
Lower nasal quadrant
36
37. keratomalacia
Stromal defects occurs due to
colliquative necrosis
Small ulcers occurs
peripherally
Circular, steep margins & are
sharply demarcated
37
38. Corneal scars
Healing of stromal
defects results in
corneal scars of
different densities &
sizes which may or
may not cover the
pupilarry area.
38
40. SKIN CHANGES
Dry, lustureless appearance occurs
Phrynoderma results: occurs due to plugging of
hair follicles by keratotic plugs ,
which consist of keratinised epithelium
projecting outwards from follicles.
Skin -> scaly & toad like.
Seen on outer side of legs, buttocks, elbow &
back of forearm
40
43. TREATMENT
LOCAL OCULAR THERAPHY VITAMIN A
Artificial tears Oral administration is
(0.7% hydroxypropyl methyl recommended
cellulose or 0.3 %
hypromellose) In case of side effects, IM
• Should be instilled every 3-4 injections of water miscible
hours preparations prefered
43
46. SHORT TERM
APPROACH
Infants 6-12 months old & any older 1,oo,ooo IU orally every 3-6 months
children who weigh less than 8 kg
Children over 1 yr & under 6 yrs of age 2,00,000 IU every 6 months
Lactating mothers 20,000 IU at delivery
Infants less than 6 months not being 50,000 IU orally- should be given
breast fed before they attain 6 months of age
46
47. A revised schedule being followed in india since 1992,
under the programme named as “CHILD SURVIVAL
AND SAFE MOTHERHOOD” is as follows
AT 9 MONTHS OF AGE
FIRST DOSE (1 LAKH IU) ALONG WITH MEASLES
VACCINE
AT 18 MONTHS OF AGE
SECOND DOSE(2 LAKH ALONG WITH BOOSTER
IU) DOSE OF DPT/OPV
THIRD DOSE(2 LAKH IU) AT 2 YEARS OF AGE
47
48. MEDIUM TERM APPROACH:
food fortification with vitamin A
• LONG TERM APPROACH:
promotion of adequate intake of
vit A rich foods.
nutritional health education
48
51. VITAMIN D
it is also called SUNSHINE VITAMIN.
it is available in 2 forms
D3 – cholecalciferol
D2 - ergocalciferol
Cholecalciferol (vitamin D3)
is made from 7-dehydrocholesterol in the skin of
animals and humans.
Ergocalciferol - D2
obtained artificially by irradiation of ergo- sterol
51
52. chemical origins of vitamin D
Precursors of vitamin D are found in both yeast and animal tissues.
In yeast, a sterol precursor (ergosterol) is converted to vitamin D2
(ergocalciferol).
In the dermal tissue of animals, the precursor is 7-dehydrocholesterol which
is converted first to a pre-vitamin D3, then to vitamin D3 (cholecalciferol).
Vitamin D2 and vitamin D3 are both converted to similar active compounds
(calcidiol and calcitriol) in the liver and kidney.
D2 and D3 are sometimes referred to as vitamers.
52
59. vitamin D - deficiency
RICKETS Children's
OSTEOMALACIA Adults
Increase the risk of Osteoporosis
59
60. Rickets
Rickets derived from the old English word for "twist," or "wrick,“
Rickets is caused by a deficiency in vitamin D.
During growth, human bone is made and maintained by the interaction of
calcium, phosphorus, and vitamin D. Calcium is deposited in immature
bone (osteoid) in a process called calcification, which transforms immature
bone into its mature and familiar form.
In order to absorb and use the calcium available in food, the body needs
vitamin D. In rickets, the lack of this important vitamin leads to low
calcium, poor calcification, and deformed bones.
60
62. X-ray in rickets
Knock knee deformity Bowleg deformity Wrist enlargement Scoliosis
Rib beading Harrison's sulcus
(rachitic rosary and pot belly Chest deformity Frontal bossing
62
63. Osteomalacia
it is also known as adult rickets
Flat bones and diaphysis of long bones are affected
it is most commonly seen in post menopause female
with history of low dietary calcium intake.
The majority of patient have bone pain &muscle
weakness..
63
64. Oral manifestation
Teeth – developmental abnormalities of dentine & enamel.
Caries – higher risk of caries
Enamel – there may be hypoplasia, may be mottled, yellow
gray in color
64
65. MANAGEMENT
Dietary enrichment of vitamin D in the form of milk
Curative treatment includes 2000 to 4000 IU of
calcium daily for 6 to 12 weeks.
osteomalacia due to intestinal malabsorption require
larger dose of vitamin D & calcium i.e.
40,000 to 1,00,000 IU of vitamin
D
15 to 20 gms of calcium lactate .
65
70. Tocopherol or vitamin E
It is also called anti-aging factor.
The word tocopherol is derived from the word toco meaning
child birth and pheros meaning to bear.
It is yellow oily liquid freely soluble in fat solvent.
Tocopherol alpha,beta,gamma,lambda have been obtained
from the natural sources
70
72. DAILY RECOMMENDED DOSE
men - 8 – 10mg
women – 5- 8mg
Children – 8.3mg
Infants – 4- 5mg
72
73. ABSORPTION ,STORAGE, EXCRETION
ABSORPTION
small intestine
it is incorporated into
lipoproteins [VLDL & LDL] &
transported through the blood
stream via the lymph.
STORAGE liver & fatty
tissue
73
74. FUNCTIONS
REPRODUCTIVE FUNCTION
it has got protective effect on reproduction and
prevention of sterility.
BLOOD FLOW AND CLOTTING MECHANISM
it dilates the capillaries & enables the blood to
flow freely.
ELECTRON TRANSPORT SYSTEM -
it functions as co factor in electron transport system
74
75. Protects liver from being damaged by toxic compounds
such as carbon tetrachloride.
Prevents the oxidation of vitamin A and carotenes.
75
76. DEFICIENCY
REPRODUCTIVE – abortion of fetus in females & atrophy
of spermatogenic structure in males leading to permanent
sterility.
HEART - there is necrosis & fibrosis of heart muscle.
BLOOD CAPILLARIES – may lead to degenerative changes
in the blood capillaries
76
77. ORAL MANIFESTATION –
loss of pigmentation ,
atrophic degenerative changes in enamel
OCULAR MANIFESTATION
PTOSIS, OPHTHALMOPLEGIA AND PIGMENTED
RETINOPATHY
77
78. MANAGEMENT –
vitamin E is given in the doses of
100 to 400mg.
78
80. VITAMIN K (PHYLOQUINONE)
It is essential for production prothrombin & other factor
involve in blood clotting mechanism.
Hence it is known as anti – hemorrhagic vitamin.
it is also known as PHYLOQUINONE
80
81. Forms
It is available in 3 forms - NAPHTHOQUINONE
K1 – it is the form occurs in
plant origin.
K2 –is synthesized by
intestinal bacteria.
K3 - synthetic form
81
85. FUNCTIONS
it is essential for the hepatic synthesis of coagulation factor II,
V, VII, IX, X.
CLOTTING – it prevents hemorrhage only in cases when
there is defective production of prothrombin
Serves as a essential cofactor in carboxylation of glutamic
acid residues in vit k dependent proteins
85
87. DEFICIENCY
Causes
Decrease
synthesis of
factor 2,7,9,10 Increase clotting time
After antibacterial Prolong bleeding
therapy,
Surgical operations-
Cholecystectomy Hemorrhagic
Conditions like
Malabsorption conditions
Obstructive
jaundice
87
88. SYMPTOMS OF VIT K DEFICIENCY
Bruising from bleeding into the skin
Nose bleeds
Bleeding gums
Bleeding in stomach
Blood in stool
Black tarry stool
Extremly heavy menstrual bleeding
Intracranial bleeding
NEWBORNS: . HEMORRHAGIC DISEASE OF
NEWBORN
. HYPOPROTHROMBINEMIA
88
89. MANAGEMENT
Vit k can be given orally
In case of someone who improperly absorbs fat or at
risk of excessive bleeding, can be given im
In case of associated liver disorder, vit k is
insufficient , blood transfusion may be neccesary
All newborns are recommended to give vit k IM to
prevent intracranial bleed after delivery
89