Detail about vit D and calcium

2. Vitamin D
 Fat-soluble vitamin.
 Stable to heat, acid, alkali & oxidation.
 Bile necessary for absorption.
 Sources
 Foods
○ Naturally found in very few foods
○ Added to many foods on the market
 Supplements
 Sunlight

3. Vitamin D
 Daily Recommended Intake
 Current minimum intake recommendations
○ Birth-50 years = 200 IU
○ 51-70 years = 400 IU
○ 71+ years = 600 IU
 Currently being debated

4. So..Exposure to Sun and Then,
Fortified Foods….Give Us the D We
Need

6. Food Sources of Vitamin D
3 oz smoked salmon = 583 IU
3 oz light tuna, canned in oil = 229 IU
1 large, whole egg = 29 IU

7. Vitamin D. is a group of sterols having
similar physiologic activity.
Forms:
D2-calciferol is activated ergosterol
(plant origin).
D3 is activated 7-dehydrochelesterol in
skin (animal origin)

8. Vitamin D
Chemical nature and properties
﹡types：VitD2（Ergocalciferol）
VitD3（Cholecalciferol ）
﹡pro-VitD2：Ergosterol
Pro-VitD3： 7-hydro-cholesterol
Ergosterol→VitD2
cholesterol→7-hydro cholesterol→VitD3
﹡active form of VitD3： 1, 25- (OH)2-VitD3
transportation: DBP

9.  Vitamin D3 is naturally present in human
skin, the provitamin (7-
dehydrocholesterol ) is activated photo
chemically to vitamin D3 which is then
transferred to the liver. Both vitamin D2
& D3 are hydroxylated (activated) in the
liver to 25-OH-cholecalciferol &,
subsequently, in the renal cortex to 1,25-
dihydroxycholecalciferol, which
functions as a hormone

14. Vitamin D Functions
 Many uses in the body
 Promotes absorption of calcium from the small
intestine
 Maintain blood levels of calcium and phosphate
for bone formation, mineralization, growth, and
repair
 Improves muscle strength and immune function
 Reduces inflammation

15. The vitamin D form, 1,25-
dihydroxcholecalciferol [1,25(OH)2D3],
 1. stimulates the synthesis of the epithelial calcium
channels in the plasma membrane calcium
pumps , and
 2. induces the formation of the calbindins.

16. Once joined with ingested vitamin D,
facilitate increased serum calcium levels .
Shows Expressed Calbindins and How
the facilitate transport of Calcium through
the Membranes

17. % 70 inorganic matrix composed
of Calcium Salts in
Hydroxyapatite
Ca10(PO4)6(OH)2.
The skeleton is resevoir for the
minerals Calcium (and
phosphorous).
Resorption: the process of
dissolving bone and releasing
its minerals into the blood for
other uses. The
OSTEOCLAST secretes ACID
PHOSPHATASE or
sometimes HCL to digest
bone matrix. Secreted by
lysosomes.

18.  It regulates absorption of Calcium and
phosphorus from renal tubules.
 It Regulates level of serum alkaline
phosphatase, which is believed to be
concerned with calcium phosphate
deposition in bones & teeth.

19. Calcium Functions
 Major component of bones and teeth
 A small amount of calcium circulates in the
blood
 Essential for clotting of the blood
 Aids in the normal functioning of the nerves,
muscles, and heart

20. Correction for Hypocalcemia

21. Vitamin D Deficiency
 At risk populations
 Breastfed infants
 Older adults
 People with limited sun exposure
 Darker skin pigments
 Certain religious groups

22. Causes
 Inadequate sun exposure
 Sunscreen use SPF>=8
 Pigmented skin
 Aging (older than 65 years)
 Winter season
 Northern latitudes above 40°
 Decreased absorption
 Bowel bypass surgery
 Crohn’s disease
 Celiac disease
 Fat and cholesterol absorption inhibitors

23. Other Causes
 Breastfeeding
 Liver failure
 Chronic renal disease
 Medications; Steroids decrease half life
of vitamin D. Dilantin, Phenobarbital,
and Rifampin can induce hepatic p450
enzymes to accelerate the catabolism of
vitamin D.

24. Calcium Deficiency
 At risk populations
 Children and youth
 Post-menopausal women
 Elderly
 People with poor diets, lacking in dairy foods

25. Vitamin D Related Diseases
 Rickets
 Osteomalacia
 Osteoporosis

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Rickets
Rickets is a general disorder of metabolism affecting
chiefly the growing bones due to deficiency of vitamin
D
Skeletal muscles & sometimes the nervous system are
also affected .
The essential changes in bones are:
1) Decalcification of the normal bones already present.
2) Formation of imperfectly calcified new bone resulting
in widening & enlargement of the epiphyseal end of the
bone .

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Etiology of Rickets
Deficiency of vitamin D (infantile Rickets).
Defective absorption of vitamin D & calcium
(malabsorption syndromes).
Hepatic diseases (biliary atresia).
Use of anticonvulsants as the combination of
phenobarbitone & phenytoin (these drugs accelerate
degradation of vitamin D by the liver).

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Etiology of Rickets
Renal diseases:
1) Defective 1-Alfa-hydroxylase enzyme
(vitamin D dependant rickets type 1 ).
2) Glomerular ( renal osteodystrophy in CRF)
3) Tubular:
- Renal tubular acidosis
- Fanconi syndrome
End organ unresponsiveness (vitamin D dependant
rickets type 2 ).

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Clinical Manifestations
Symptoms:
Early (between 3-6 months)
- head sweating.
- irritability by day & sleeplessness by night.
Advanced rickets:
- delayed motor development (sitting, standing & walking).

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Signs:
1) Bony Changes:
Changes in the skeleton are greatest @ the sites where growth is most rapid
& the deformities are the result of gravity & traction of muscles on the
affected bones.
A. Head:
1) Anterior fontanel: is wider & its closure is delayed than normal.
2) Frontal and parietal bossing:.
3) Head size: looks larger than normal.
4) Head shape: the vault & occiput are flattened [this together with frontal &
parietal bossings & the grooves between the bosses result in caput
quadratum (the skull is square)].
6) Teeth eruption: is usually delayed & deciduous teeth may show enamel defect
or decay.

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B. Thorax:
1) Rachitic rosary: beading of ribs @ costochondral junctions is
another early sign & is seen as a row of nodules about the size of
cherries extending down & backwards along the line of
costochondral junctions.
2) Harrison sulcus: is a horizontal groove corresponding to the line of
attachment of the diaphragm with flaring of the costal margin
below.

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C. Extremities:
1) Epiphyseal enlargement: is common & best felt @ the wrists & ankles.
2) Marfan’s sign: is a transverse groove that is felt over the malleoli just
proximal to the ankle join. It is due to the excess osteoid tissue deposited
in the centers of ossification of the lower ends of tibia & fibula &the
malleoli.
3) Deformities: tibia & fibula often become curved after the rachitic child has
started to walk resulting in bow legs or knock knees. The femur & tibia
may show an anterior convexity. The humerus & the bones of the forearms
may show convexity on their extensor surfaces as the infant crawls.
4) Fractures: of the green stick variety are often seen.

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D. Pelvis:
The pelvis in rickets is small & continue to be retarded in growth. The
pelvis inlet is narrowed by a forward projection of the promontory of the
sacrum & the outlet is narrowed by a forward projection of the tip of the
coccyx . In females, these changes , if they become permanent , add to the
hazards of the childbirth & may necessitates C/S.

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2) Muscle & Ligaments:
Hypotonia of the muscles & laxity of the ligaments are usually present, they
lead to the following:
1. Delayed motor milestones as sitting & walking.
2. The abdomen is distended due to:
- Hypotonia of the abdominal muscles & the muscles of the intestines.
- Downward displacement of the liver & spleen due to Hypotonia of
abdominal muscles, laxity of their ligaments & the deformity of the chest
wall.

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Complication of Rickets
Tetany:
(the most important complication. It is usually precipitated by
infections).
Recurrent chest infections due to:
1) Chest wall deformity.
2) If there is associated vitamin A deficiency (vitamin A is essential
for the integrity of epithelial surfaces including respiratory
mucosa).
3) Defective function of the immune system may occur (especially T
lymphocytes).
Bone fractures.
Bone deformities.

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Biochemical Changes in
Rickets
 Serum Ca is normal (2ry to compensatory hyperparathyroidism).
 Serum PO4 is decreased (2ry to compensatory hyperparathyroidism).
 Alkaline phosphatase in blood is increased.
 Decreased 1,25-dihydroxy vitamin D in the serum.

40. Osteomalacia or Adult
…………...Rickets
 Vitamin d deficency in adults is rare due
to sun exposure and ability of skin to
synthesized it from 7-dehydrocholestrol.
 May occur in pregnancy and lactation in
which vitamin demand is increased
 Repeated pregnancies is also a cause.

41. Clinical Effects
 Softing and easy fructure of long bones
may occur.
 Pelvis bone effected the most causing
birth difficulties

42. Vitamin D and Cancer
 Roles in prevention of
 Colon cancer
 Breast cancer

43. Vitamin D and Cancer
 How it prevents
 Promotes cellular differentiation
 Decreases cancer cell growth
 Stimulates cell deaths

44.  Role in Cardiovascular Diseases
 Vitamin D deficiency activates the renin-
angiotensin-aldosterone system and can
predispose to hypertension and left ventricular
hypertrophy.
 Additionally, vitamin D deficiency causes an
increase in parathyroid hormone, which
increases insulin resistance secondary to
down regulation of insulin receptors and is
associated with diabetes, hypertension,
inflammation, and increased cardiovascular
risk.

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Effects of Excess
 Wide variation in tolerance, over 500ug/day toxic when continued for
weeks, prolonged administration of 45ug/day may be toxic.
 Nausea.
 Diarrhea.
 Weight loss.
 Polyuria.
 Nocturia.
 Soft tissue calcification
(heart, renal tubules, blood vessels, bronchi & stomach).

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Hypervitaminosis D.
Clinical manifestation:
The patient feels weak, thirsty, anorexic & loses weight.
Nausea & vomiting.
Polydepsia & Polyuria.
Constipation.
Dehydration.
Kidneys (stone formation or nephrocalcinosis which may lead to
renal failure.
Deposition of Ca in soft tissues around the joints & in the walls of
blood vessels. Metastatic calcification may occur in the heart,
lungs, thyroid & pancreas.

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Laboratory findings:
 Serum Ca increases.
 Serum phosphorus is normal. It increases in renal failure.
 Urinary Ca increases.
Radiological findings:
 Increased density of bones @ the growing ends.
 Dense metaphyseal lines.
 Ca deposition in soft tissues.
 U/S scan for renal stones or nephrocalcinosis.

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Treatment:
 Stop administration of vitamin D.
 Correct dehydration.
 Decrease calcium in diet by stopping milk & its products or by increasing
cereals in the diet to decrease calcium absorption .
 Prednisone 2mg/kg/day is an effective antidote, it should be given until the
serum Ca has fallen to 12mg/dl, then it should be stopped.