Fat-soluble vitamins are absorbed through the intestinal tract with the help of lipids Fat-soluble vitamins are absorbed through the intestinal tract with the help of lipids , dental seminar,

1. Vitamin E & K
Dr. Parvin Rajulu B
Dept. of Oral & Maxillofacial Pathology

2.  Fat-soluble vitamins are absorbed through the intestinal
tract with the help of lipids (fats).
 Because they are more likely to accumulate in the body,
they are more likely to lead to hypervitaminosis than are
water-soluble vitamins.
 Small amounts of vitamins A, D, E and K are needed to
maintain good health.
 Foods that contain these vitamins will not lose them when
cooked.
 The body does not need these every day and stores them in
the liver when not used.
 Most people do not need vitamin supplements.
 Megadoses of vitamins A, D, E or K can be toxic and lead to
health problems.
Some
facts:

4. VITAMIN E
 Discovered By EVANS and BISHOP, as a fat soluble
factor.
 This factor was named Vitamin E and given the generic
name of TOCOPHEROL which means ‘the alcohol
which brings forth offspring.”

5.  Several compounds belonging to the tocopherols have been
shown to exhibit Vit. E activity.
 α-tocopherol has the highest biological activity & widest
distribution.
 It is an alcohol which has phytol & trimethylhydroquinone in
its structure.

6. Sources:
 Sunflower, safflower, soya bean,
corn oils.
 Meats, nuts and cereal grains.
 Milk, milk products, egg yolk.
 Green leafy vegetables.
 Diets high in polyunsaturated fats may need a slightly
higher requirement for Vitamin E.

7. Recommended daily allowance:
 Depends on intake of PUFA (nearly 0.4 mg/g of PUFA).
 3 mg for infants to 10 mg for adult males.
 Normal: 5-10 mg/ day.
 Increased intake in pregnant and lactating women is
suggested, especially in view of the low perinatal Vitamin
E levels in the infant.
 Vitamin E has gained lot of attention in the last decade
because of its role as a PUFA antioxidant.

8.  One of the prevailing theories of aging states that aging
is, in part, a progressive accumulation of cellular damage
resulting from free radicals.
 As an antioxidant,Vitamin E may play a role in the
prevention of free radical damage.
 High doses of Vitamin E may reduce platelet aggregation
and interfere with Vitamin K metabolism.

9. Absorption & metabolism:
 Vit. E is readily absorbed from the GIT with fats & is
transported in lipoproteins to liver and peripheral tissues.
 It is also concentrated in phospholipids.
 Levels of Vit. E in the plasma lipoproteins &
phospholipids depends on:
 Dietary levels of Vit. E
 Various pro- & antioxidants
 Se and S containing aas.

11. Biological role:
 Vit. E has strong antioxidant properties particularly for
the lipids & is involved in metabolism with Se.
 Both Vit. E and Se are interdependent in preventing lipid
peroxidation & in sparing Vit. A and PUFA.
 Regulates requirement of Se by preventing its loss from
from body helps in maintaining its active form.

13.  Vitamin E acts as a chain breaking antioxidant and is an
efficient free radical scavenger, which protects low
density lipoproteins and polyunsaturated fats in
membranes from oxidation.
 A network of other antioxidants and enzymes maintains
Vitamin E in a reduced state.
 Vitamin E also inhibits Prostaglandin synthesis and the
activities of Phospholipase A2.

15. DEFICIENCY
 Dietary deficiency of Vitamin E does not exist.
 Vitamin E deficiency is seen in only severe and prolonged
malabsorptive diseases or after small intestinal resection.
 Seen in children with fat malabsorption
 Children with Cystic fibrosis may develop Vitamin E
deficiency characterized by hemolytic anemia.

16. Deficiency may cause:
 Sprue,
 Creatinuria
 Peptic ulceration
 Abnormal red cell hemolysis & their diminished life
span.
 Reproductive defects
 Muscular dystrophy
 Vascular system defects

17. Clinical features:
 Vitamin E deficiency causes axonal degeneration of the
large myelinated axons and results in spinocerebellar
symptoms (ataxia).
 Peripheral neuropathy is initially characterised by
areflexia, with progression to an ataxic gait and by
decreased vibration and position sensations.

19. VITAMIN K
 Name derived from German word, Koagulation, because
of its important role in blood clotting.
 Various compounds related to 2-methyl-1, 4-
napthoquinone have been described to have Vit. K
activity.

20. There are two natural forms of Vitamin K:
 Vitamin K1
 Vitamin K2
 Both have a naphthoquinone ring & an aliphatic side chain.
 Vitamin K1 (Phylloquinone, phytominadione, phytonadione)
isolated from plants, has phytyl side chain.

21. Vitamin K2
MKn 
 Vitamin K2 (Menaquinone) which is synthesized by
intestinal bacterial flora and found in hepatic tissue.
 It has a side chain with isoprenoid units.
 Is water soluble and gets easily absorbed on parenteral
administration.
 Most biologically active form.

22. Vitamin K3 or MENADIONE
 It is a chemically synthesized provitamin that can be
converted to menaquinone by the liver.
 Available commercially for therapeutic uses.

23. Absorption:
 Absorbed with dietary
fats in the presence of
bile salts.
 Utilized in liver after its
absorption.

24. Biological role:
 Maintains normal levels of some blood clotting factors:
Post- translational modification of clotting factors II, VII,
IX, X (convert them to biologically active form).
 The reduced form of Vitamin K causes carboxylation of
glutamic acid residues present in these clotting factors.
 The γ-carboxyglutamic acid residues of these clotting
factors combine with positively charged Ca++ to form a
complex.

25.  The Prothrombin-Ca
complex binds to the
phospholipids on the
membranes of the platelets,
leading to an increased
conversion of prothrombin
to thrombin.
 Warfarin type drugs inhibit
this γ-carboxylation by
preventing the conversion of
Vitamin K to its active form.
Protein-Ca-phospholipid interaction 

26.  Vit. K antagonists (Warfarin- coumarin derivative,
heparin), act as competitive inhibitors of the enzymes
concerned with the activation of prothrombin and other
coagulation factors which require Vit. K as coenzyme.

27. SOURCES
PLANT SOURCES:
 Green leafy vegetables, vegetable oils such as olive and
soya bean oil.
ANIMAL SOURCES:
 Butter, liver, milk, egg yolk.

28. Requirement:
 20-100 μg/day for adults.
 1mg, prophylactic dose to newborns
on 1st day after birth.

29. Deficiency causes:
 Deficiency symptoms of Vitamin K are due to hemorrhage.
 Newborns are particularly susceptible due to low fat stores,
liver immaturity and poor placental transport. Also
intestinal flora not fully developed.
 Intracranial as well as gastrointestinal and skin bleeding
can occur in Vitamin K deficient infants 1-7 days after birth.
 Thus, Vitamin K  1 mg I.M. is given prophylactically at the
time of delivery.

30. Deficiency may cause spontaneous bleeding, ecchymosis
& hemorrhage.

31. Oral manifestations:
 Excessive gingival bleeding may occur after a surgical
procedure.
 Spontaneous bleeding may occur if prolonged deficiency
is present.

32.  Delayed Prothrombin time & hemorrhagic tendency, in
patients with:
 Malabsorption (sprue)
 Chronic small intestinal disease
 Obstructive jaundice (obstructed biliary tracts)
 Advanced hepatic damage (liver Ca, cirrhosis etc.)
 After small bowel resection
 Anticoagulant therapy
 Those on broad spectrum antibiotics (by reducing gut
bacteria, which synthesize menaquinones, and by
inhibiting the metabolism of Vitamin K).

33.  Diagnosis of Vitamin K deficiency is usually made on
the basis of :
An elevated PT or reduced clotting factors.
 Vitamin K deficiency is treated using a parenteral dose of
10 mg.
 For patients with chronic malabsorption,
 1-2mg/day of Vitamin K should be given orally, or
 1-2 mg/week can be taken parenterally.

34. Therapeutic preparations:
 Phytonadione (VITAMIN K1)
 Menadione (VITAMIN K3)
 Aquamephyton-I.M.,S.C.
 Mephyton-I.M.
 Konakion-I.M.
 Synkayvite (Menadiol sodium diphosphate)
 Vitamins K1 AND K3 are available as part of
multivitamin complexes or alone as 5 mg tablets.

35. Thank you!!!