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1
Q

….
…vitamins are a group of sterols that have a hormone-like function.

A

Vitamin D:

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2
Q

Vitamin D:

The active form

A

1,25-dihydroxycholecalciferol or calcitriol binds to intracellular receptor proteins.

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3
Q

The most prominent actions of 1,25-diOH-D3 are to regulate the

A

plasma levels of calcium & phosphorus .

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4
Q

Distribution of Vitamin D:

A
  1. Endogenous vitamin D precursor:
    • Cholesterol → 7-Dehydrocholesterol —-→ cholecalciferol in dermis & epidermis by UV of sunlight, then it’s transported to liver bounded to vitamin D–binding protein.
  2. Diet: Ergocalciferol (vit. D2), found in plants
    & cholecalciferol (vit. D3), found in animal tissues, are sources of preformed vitamin D activity. They are packaged into chylomicrons → lymphatics → blood.
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5
Q

Metabolism of Vitamin D:
Formation of 1,25-diOH-D3 (Calcitriol): Vitamins D2 & D3 are NOT biologically active converted in vivo to the active form of D vitamin by

A

by two sequential hydroxylation (OH) reactions:
a. The first (OH): occurs at the 25-position, in the liver, producing 25-hydroxycholecalciferol( ( predominant form of
vitamin D in plasma and the major storage form of the vitamin. ))

b. The second (OH): occurs at position 1 in kidney, producing
1,25-diOH-D3 (calcitriol) by 1-hydroxylase enzyme.

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6
Q

Regulation of 1-Hydroxylase enzyme

A

The enzyme activity is ↑directly by ↓plasma phosphate or indirectly by ↓ plasma calcium which stimulate secretion of PTH) → ↑the activity of 1 hydroxylase,
Calcitriol →inhibits synthesis of PTH.
→ inhibits the activity of 1-hydroxylase.

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7
Q

Functions of Vitamin D: calcitriol (1,25-di[OH]D ), acts as a hormone. Why?

A

Together with PTH, it plays a role to increase plasma level of Ca:
+It is also important for cell differentiation.
-increase ca & PO mobilization from bones (need PTH).
-decreased Ca excretion from the kidney , increased reabsorption (with PTH
-Calcitriol alone increased ntestinal absorption of Ca. It binds to a cytosolic receptor forming a complex which moves to the nucleus to interact with the DNA → ↑calcium uptake.

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8
Q

▪Vitamin D occurs naturally in

A

fatty fish, liver and egg yolk. ▪Milk is not a good source of the vitamin D.

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9
Q

Vitamin D deficiency → demineralization of bone

A

rickets in children & osteomalacia in adults.

High risk patients are: o Infants and elderly lacking sunlight and/or ↓
in vitamin D consumption, fat malabsorption.

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10
Q

Vitamin D Toxicity:

A

loss of appetite, nausea, thirst and stupor.

Enhanced calcium absorption & bone resorption → hypercalcemia →deposition of Ca in many organs, particularly the arteries & kidneys.

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11
Q

Vitamin D Deficiency:

A
  1. Nutritional rickets:
    a. Rickets:
    oInadequate calcification.
    oMisshapen, deformed bones.
    oLax muscles with spas
    b. Osteomalacia:
    o Demineralization of bones.
    o Soft, deformed bones.
    o Pain, weakness & ↑
    susceptibility to fracture.
  2. Renal Osteodystrophy:
    Chronic kidney disease → ↓ ability to form active vitamin D & ↑ retention of PO → hyperphosphatemia and hypocalcemia.
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12
Q

sources of vitamin E,

A

Polyunsaturated plant oils are rich sources of vitamin E,
while liver & eggs contain moderate amounts.

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13
Q

The E vitamins consist of

A

eight naturally occurring tocopherols, of which α-tocopherol is the most active.

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14
Q

Functions of Vitamin E: ▪Chief function in the body is as

A

antioxidant → stops the production of reactive oxygen species (ROS)
o Stabilization of cell membranes,
o Regulation of oxidation reactions,
o Protection of polyunsaturated fatty acids and vitamin A.

▪It is important for the proper function of nerves and muscles.

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15
Q

Antioxidants include

A

Vitamins E, Vitamins C, Selenium, Carotenoids
& Flavonoids.

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16
Q

Vitamin E Deficiency May Results in:

A

Vitamin E ↓ is almost entirely restricted to premature infants.

In adults, the deficiency is usually associated with defective lipid absorption or transport (e.g. patients with biliary, pancreatic & intestinal diseases that is characterized by excessive steatorrhea).

Vitamin E Deficiency May Results in:
1. Sensitivity of RBCs to peroxides → hemolytic anemia.
2. Damage of nerves, loss of reflexes, muscle weakness & ataxia.
3. Atherosclerosis.
4. May ↑
risk of certain cancers.

17
Q

Vitamin K: It is required for the synthesis of

A

It is required for the synthesis of certain proteins necessary for blood coagulation.
synthesis of “bone calcium-binding proteins” to manipulate binding of Ca in bone and other tissues.

18
Q

Vitamin K: produce by
Storge,Absorption

A

▪Intestinal bacteria produce ~75% of Vitamin K absorbed daily. ▪Vitamin K is not stored in the body. So, it needs to be supplied daily. ▪Absorption depends on healthy liver and gall bladder.

19
Q

Vitamin K is a Quinone derivative occurring as:

A
  1. Vitamin K 1 (phylloquinone): produced by plants.
  2. Vitamin K2 (menaquinone): produced by intestinal bacteria.
  3. Synthetic Vitamin K (menadione), water soluble derivative for therapy and can be converted to K 2

Vitamin K is the more potent ,15X more active than K1

20
Q

Vitamin K Functions:

A
  1. Formation of γ-Carboxyglutamate (Gla)

In liver, blood clotting factors II (prothrombin),
VII, IX, & X are synthesized as inactive precursor molecules that contain glutamic acid residues.
This needs vit. K as a coenzyme
This is inhibited by dicumarol & warfarin

  1. Interaction of Prothrombin with Membranes: Prothrombin and other blood clotting proteins each contain between 4-6 Gla which chelate calcium ions,
  2. γ-Carboxyglutamate Residues in Other Proteins:
    Osteocalcin of bones.
    Proteins S & C: involved in limiting the formation of blood clots →control & regulate blood clotting.
  3. Other Functions of Vitamin K:
    o Integration of Ca into bones.
    o Prevent Ca deposition in blood vessels (vascular calcification).
    o Maintain blood vessel elasticity.
21
Q

Sources of Vitamin K & Deficiency:

A

Sources:
o Cabbage, cauliflower, spinach, egg yolk and liver. o Synthesized by intestinal bacteria flora.
▪Deficiency:
o No true vitamin K deficiency
o Some antibiotics ↓ intestinal flora → ↓ vitamin K synthesis. -bleeding/hemorrhage & So → prolonged
prothrombin time (PT). Therefore, PT & PTT (Partial Thromboplastin Time) are ↑.
-weaken bones and promote calcification of arteries & other soft tissues.
High risk groups:

  1. Newborns particularly prematures. So given a single IM dose of vitamin
    K at birth as a prophylaxis against hemorrhagic disease. 2. Fat malabsorption. 3. Consumption of unabsorbed lipids.
22
Q

Vitamin K Toxicity:

A

hemolytic anemia and jaundice in the infants, due to toxic effects on the membranes of RBCs.

23
Q

Vitamin K & Anticoagulants:

A

▪ Warfarin, an anticoagulant, blocks the regeneration of active vitamin K.
▪ Broad spectrum antibiotics like neomycin alter the intestinal flora → ↓
vitamin K production.