vitamins

1. VITAMIN A
• fat-soluble micronutrient
• Biologic activity of all trans-retinol
• Vitamin A -from the diet as retinyl esters, such as
retinyl palmitate, which are called preformed
• vitamin A.
• found primarily in certain foods of animal origin.
• other sources: several provitamin A carotenoids,
which are
• found naturally in many fruits and vegetables,
• β-carotene.

2. RETINOL
RETINAL
RETINOIC ACID

3. METABOLISM OF VITAMIN A
• ANIMALS
PRODUCTS
• RETINAL
ESTERS
• RETINOL
• PLANTS
• RETINAL
• RETINOL

4. STORAGE IN LIVER
TRANSPORTED IN LIVER BY BLOOD
PACKAGES IN CHYLOMICRONS
RETINYL ESTERS
RETINOL

5. PERIPHERAL TISSUES
RELEASE OF RETINOL WITH RBP;TTR

6. FUNCTIONS
HOST RESISTANT
TO INFECTIONS
REPRODUCTION
GROWTH AND
DIFFERENTIATION
OF TISSUES
VISION

7. Vitamin A Deficiencies
• NIGHT BLINDESS
• XEROPTHALMIA/DRY
EYE-Bitots spot
• KERATOMALACIA
OCCULAR
• SQUAMOUS METAPLASIA
• TOADS SKIN
• Faulty epiphyseal bone formation
• Defective tooth enameL
NONOCUULAR

8. Diagnosis
• In children, plasma retinol values
• of <0.35 μmol/L are considered to be very deficient, 0.35-
0.7 μmol/L
• are considered to be deficient, 0.7-1.05 μmol/L are
considered to be
• marginal, and >1.05 μmol/L are considered to be adequate.
It has long
• been thought that the liver vitamin A concentration must
be 20 μg/g
• or higher to support a normal rate of secretion of retinol-
RBP into
• plasma.

9. • AGE RANGE
• RECOMMENDED DIETARY
• ALLOWANCE (RDA) (μg retinol
• equivalents per day)
• UPPER LEVEL (UL)
• (μg retinol equivalents
• per day) COMMENTS
• 0-6 mo 400 600 The recommended intake for infants is an adequate intake,
• based on the amount of vitamin A normally present in
• breast milk
• 7-12 mo 500 600
• 1-3 yr 300 600 The UL applies only to preformed vitamin A (retinol).
• 4-8 yr 400 900
• 9-13 yr 600 1,700
• 14-18 yr 900 male; 700 female 2,800

10. Vitamins D
• ERGOCALCEFEROL
• CHOLECALCEFEROL FROM 7 DEHYDRO

11. Rickets
disease of growing bone that is caused by
unmineralized matrixCRANIOTABES
RACHITIC
ROSARY
Harrison
groove

12. • Rachitic changes
• Fraying, Cupping
• Coarse trabeculation of the diaphysis
RADILOGICAL
• Based on radiologic findings.DIAGNOSIS
• Cutaneous synthesis of Vit D3
• maternal risk factors
• child’s medication
• Malabsorption
• A history of renal disease
• The family history
Clinical
Evaluation

13. Cutaneous synthesis
Food sources
Transport:
25-hydroxyvitaminD(25-D)-
LIVER
1, 1, 25 D-KIDNEY
1,25-D
Ca absorption
Bone resorption
Suppresses PTH secretion(PT
gland)
(-)its own synthesis
in kidney
Increases synthesis of
inactive metabolites
PHYSIOLOGY

14. Etiology
• Infancy(poor intake
and inadequate
cutaneous synthesis)
laboratory

15. Clinical manifestation
GENERAL
-Failure to thrive
-Listlessness
-Protruding abdomen
-Muscle weakness
(especially proximal)
-Fractures
HEAD
-Craniotabes
-Frontal bossing
-Delayed fontanel
closure
-Delayed dentition;
-Craniosynostosis
CHEST
-Rachitic rosary
-Harrison groove
-Respiratory
infections and
atelectasis

16. Clinical manifestation
BACK
-Scoliosis
-Kyphosis
-Lordosis
EXTREMITIES
Enlargement of wrists and
ankles
Valgus or varus deformities
Windswept deformity
Anterior bowing of the tibia
and femur
HYPOCALCEMIC
SYMPTOMS
-Tetany
-Seizures
-Stridor due to
laryngeal spasm

17. Treatment
• 300,000-600,000 IU of vitamin D are
administered orally or intramuscularly as 2-4
doses over 1 day.
• Daily high dose of 2,000-5,000 IU/day over 4-6
wk.
• Either strategy should be followed by daily
vitamin D intake of 400 IU/day if <1 yr old or
600 IU/ day if >1 yr old.

18. • Most cases of nutritional rickets can be
prevented by universal administration of 400
IU of vitamin D to infants who are breastfed.
Older children should receive 600 IU/day.

19. hypervitaminosis
etiology pathogenesis manifesation

22. • hypercalcemia and extremely elevated levels
of 25-D (>150 ng/mL)
• Hypercalciuria leading to nephrocalcinosis