This slide deals with different aspects of vitamin A sources, their deficiency syndromes particularly in Animals

1. Welcome to presentation
Vitamin A

2. Overview
Vitamin A occurs as retinol, retinoic acid,
and retinal. It is a fat-soluble compound.
Together with its precursors, the carotenoids,
it is highly labile and rapidly destroyed by
light, oxygen, heat, and acid.

3. Overview
Vitamin A is required by all mammals and is
synthesized through the metabolism of
carotenoid precursors (carotenes) present in
Leaves and some grains.

4. Absorption
The proximal jejunum is the primary site of
vitamin A and carotene absorption. A normal
pancreatic, hepatic, and biliary function,
together with an adequate dietary fat content
and normal fat digestion and absorption, is
required for the absorption of β-carotene and
its subsequent conversion to retinol.
Ruminal microbial degradation of
biologically active vitamin A is appreciable
and varies with diet composition.

5. sources

8. Transport
• Transported via chylomicrons from intestinal
cells to liver.
• Transported to targeted tissue from liver as a
retinol through retinol binding protein, which
is bind as transthyretin.

9. Storage
• Liver is main storehouse.
• Stored as retinopalmitate
• EXCEATION
• Not readily excreted
• Execrated via urine .

10. Factors affecting vitamin A utilization
1. Environmental temperature : high temperature leads to
utilization of vitamin a
2. Ration : higher concentrate feed leads to higher
metabolism and leads to higher utization of vitamin a,and
High-concentrate diets can result in up to 70% pre-
intestinal degradation of vitamin A, whereas diets with
>75% forage result in <20% degradation, factors to be
taken into account for diet formulation and vitamin A or
β-carotene supplementation
3. Hypothyroidism :thyroxin it helps in conversion of
carotene to vitamin a .
4. Hypophostaemia : low phosphorus levels retards the
conversion of carotene to vitamin a.

11. 1. Cathartic drug :oligenous purgatives (liquid
paraffin )decreased the availability of vitamin
through excretion from gut as the vitamin is
fat soluble .
2. Nitrates and Nitrites :interfere the conversion
of vitamin carotene to vitamin A

12. General functions
1. Vitamin A is required for cellular
2. differentiation,
3. growth and development
4. adequate vision,
5. thyroid gland function,
6. protein synthesis,
7. conversion of cholesterol to
8. corticosterone,
9. glycogen synthesis,
10. Immune function,
11. regulation of gene expression,and
12. iron metabolism

13. Deficiency
1. Growth : causes poor appetite and
emaciation in growing animals .
2. Vision :
ocular signs
primary secondary

14. Primary signs :
• Conjunctival xerosis
• Corneal xerosis
• Corneal ulceration
• Keratomalacia
Secondary signs
• Night blindness
• Xeropthalmia
• Corneal scar

15. Keratomalacia
A softening and ulceration of the cornea of the
eye resulting from severe systemic deficiency of
vitamin A.

16. Night Blindness (Nyctalopia)

17. Neurologic disorder
1. Limb weakness
2. Incoordination and paralysis of skeletal
muscle .
3. Facial paralysis
4. Rotation of head

18. Congenital Anamolies
1. Anophthalmos
2. Cleft plate
3. Microphthalmos
4.

19. Bone development
1
• Vitamin a deficiency
2
• Decrease in osteoblastic activity during
growth stage
3
• Reduction in bone formation

20. Mucus epithelial cells
Deficiency of vitamin A
Loss of integrity of epithelial cells
Secretary cells are transformed to keratinized
cells
Inefficient synthesis of mucopolysacchrides

21. Epithellial cells
1. Skin :hyper keratinization of skin lead to
xerodermia
2. Alimentary tract :degenerative changes to
intestinal epithelium and secretory glands.
3. Respiratory tract : degenerative changes and
stratification of epithelium.
4. Urinary system :degeneration and cornification
of epithelium
5. Reproduction :impaired oogenesis and
spermatogenesis leads to reproductive failure

22. Toxicity
1. osteoporosis,
2. reduced feed intake
3. decreased cerebrospinal fluid pressure.
4. skeletal malformation and osteoporosis leading to
spontaneous fractures, anemia, delayed blood
clotting and internal hemorrhages, partial or total
anorexia, growth retardation and weight loss,
alopecia.
5. Skin thickening with hyperkeratosis
6. enteritis with chronic diarrhea, hepatomegaly and
splenomegaly with degenerative atrophy and fatty
infiltration of liver and kidneys,
7. conjunctivitis, and congenital abnormalities.

23. CAUSES AND RISK FACTORS
1. Poor dietary formulation with low or
excessive vitamin A and/or inadequate fat
content.
2. Low forage availability.
3. Feed exposure to light and heat or the
presence of moisture and trace minerals
accelerates the loss of vitamin A activity.

24. DIFFERENTIAL DIAGNOSES
Deficiency
Cattle: Polioencephalomalacia,
1. lead poisoning,
2. water deprivation/sodium toxicosis,
meningoencephalitis.
3. other causes of increased intracranial pressure
and blindness.
4. Small ruminants: Pregnancy toxemia and
listeriosis.

25. • Toxicity
All causes of skeletal malformations and
spontaneous fractures, hepatic lipidosis, and
renal failure

26. Treatment
Deficiency is rapidly corrected with vitamin
A supplementation (dietary and injectable).
Common dietary sources of carotenes are
carrots, yellow corn, alfalfa (legumes), green
grass (pasture, hay, or silage).
Advanced clinical signs of both deficiency
and toxicity are irreversible.