Hey guys, in this video, we will see vitamin K.
So, let’s start.
It is a fat-soluble vitamin.
There are three types of vitamin K.
K1, also called phylloquinone and phytonadione
is synthesised by plants.
Vitamin K2 is also called menaquinone and
it is synthesized by bacteria.
Commensal bacteria in our intestine
also synthesize vitamin K2.
K3 is called menadione.
It’s a synthetic analogue.
And its water soluble.
Coming to its daily requirements.
As our intestinal bacteria synthesize vitamin K, its requirement in diet is variable.
Its estimated to be about 100 microgram per
day for an average adult.
Dietary sources include, Alfalfa, spinach,
cabbage, cauliflower, other GLV,
egg yolk, meat and dairy products.
Its absorption occurs mainly from small intestine.
As its fat soluble, its absorption requires
bile salts from liver.
It is absorbed in chylomicrons along with
fat, into the lymphatic channels.
It is stored mainly in liver.
However, the storage does not occur to a larger extend
and its level declines rapidly
if it’s not taken in diet regularly.
Now the most interesting part, Function.
Vitamin K is required for synthesis of clotting
factors II, VII, IX and X.
Let’s see the detail.
Clotting factor II, VII, IX and X
have glutamic acid residues.
These residues need to be carbonylated for
proper functioning of these factors.
Gamma glutamyl carboxylase
is the enzyme for this reaction.
The reaction also requires oxygen and carbon dioxide.
Vitamin K, in its reduced-hydroquinone form,
works as cofactor in this carboxylation reaction.
In the reaction, its active hydroquinone form
is converted to oxidized (epoxide) form,
which is inactive.
To reactivate vitamin K, we have an enzyme,
vitamin K reductase.
This enzyme with help of NADH, converts
vitamin K back to its active reduced form,
which can then contribute in carboxylation of other
molecules of clotting factors.
Now the importance of this carboxylation reaction.
The carboxylation provides negative charge
to the glutamate residues.
This negative charge is essential for its
binding with calcium,
and thereby to membrane phospholipidsof platelets.
This in turn allows its interaction with other molecules,
like its own activation and subsequent participation in coagulation.
Thus, vitamin K is crucial for haemostasis.
In fact, it has derived this name because
it was initially designated as
Kagulation vitamin in German because of its role in coagulation.
Similarly, vitamin K is also required for
carboxylation of protein C and protein S,
both of which are anticoagulant factors.
Osteocalcin, found in bones, and some proteins
in kidney, lungs, placenta and spleen.
Now the deficiency.
Vitamin K deficiency is rare as its synthesized
by our intestinal bacteria
and enough quantity is usually present in diet.
Yet, it is seen in some conditions.
Like, new-borns babies.
They are susceptible to vitamin K deficiency,
because vitamin K does not cross placenta or enter breast milk in enough quantity.
They have very low stores of vitamin K. And
also, they lack intestinal microflora.
Next, Prolonged use of antibiotics can suppress
intestinal bacteria and cause vitamin K deficiency.
Conditions causing malabsorption like biliary
obstruction which impairs access to bile salts,
dysentery, enterocolitis, celiac disease,
Crohn’s disease, ulcerative colitis
and resection of intestine can also
cause vitamin K deficiency.
Hepatocellular disease can lead to
manifestations of vitamin K deficiency.
However, this is due to incapability of liver
cells to synthesize clotting factors,
rather than actual deficiency of vitamin K.
It’s very simple if you have understood its function well.
If you dont have vitamin K in your body, clotting
factors II, VII, IX and X
do not get carbonylated at glutamic acid residues.
Without it, they cannot associate with calcium,
so all the subsequent effects are lost.
This leads to impaired coagulation and increased
This manifests as bruising, ecchymosis, haematuria,
epistaxis, gastrointestinal bleeding,
intracranial bleeding, post-operative haemorrhage, and prolonged bleeding and clotting time.
Now the uses.
It is used in case of its dietary deficiency,
in new-borns, 1 mg vitamin K by intramuscular route is usually given as prophylaxis.
Poisoning with warfarin or similar oral anticoagulants
is treated with vitamin K as specific antidote.
It’s also used in case of prolonged use of antibiotics
as they might suppress intestinal flora and reduce our inhouse vitamin K synthesis.
Lastly, it can also be used along with salicylates
as they are antagonist to vitamin K
and their prolonged use at high dose can cause hypoprothrombinaemia.
By the way, prothrombin is factor II.
Now the last topic, toxicity.
Vitamin K1 and K2 which occur naturally are
Toxicity occurs mostly with vitamin K3.
It includes haemolysis, hyperbilirubinemia, jaundice etc.
especially in patients with
G6PD deficiency and new-borns.
It can precipitate kernicterus in new-born
as it causes haemolysis
and competitively inhibits glucuronidation of bilirubin.
Because of this toxicity profile, vitamin
K3 should not be used.
Thats everything for vitamin K.
Now it’s time for summery.
Vitamin K is a fat-soluble vitamin.
It occurs in 3 types.
K1 is synthesized by plants.
K2 by bacteria and K3 is synthetic and water soluble.
Its daily requirement is variable as it is
synthesized by intestinal flora.
Is about 100 microgram per day.
Dietary sources are alfalfa, spinach, cabbage, cauliflower, other GLV, egg yolk, meat and dairy products.
Absorption in intestine requires bile salts.
Storage occurs mainly in liver.
However, it declines rapidly without regular
Vitamin K is required for synthesis if clotting
factors II, VII, IX and X.
They are carbonylated by gamma glutamyl carboxylase.
The reaction converts active hydroquinone
form of vitamin K into inactive epoxide form.
Vitamin K reductase reactivates vitamin K
Carboxylation of these factors is essential
for their participation in coagulation.
Also, vitamin K is required for
synthesis of protein C and protein S
which are anticoagulant factors and osteocalcin.
Its deficiency can occur in new-borns
as vitamin K does not enter placenta
or breast milk in enough quantity,
they have low storage and do not have intestinal microflora to synthesize vitamin K.
Prolonged antibiotic use destroys
intestinal bacteria and cause deficiency.
Malabsorption obviously can
cause deficiency of any vitamin.
In hepatocellular disease patient develop
features of vitamin K deficiency at it is not utilized.
Without vitamin K there is no carboxylation
of glutamic acid residues in clotting factors
which impairs coagulation.
This increases bleeding tendency which manifests
as bruising, ecchymosis, epistaxis, haematuria,
gastrointestinal bleeding, intracranial bleeding,
and increased bleeding and clotting time.
It is used in its dietary deficiency,
malabsorption, in new-borns,
poisoning with warfarin and similar oral anticoagulants,
and prolonged use of antibiotics and salicylates.
Finally, toxicity profile.
Vitamin K1 and 2 are safe.
Toxicity usually occurs with vitamin K3.
It includes haemolysis, hyperbilirubinemia
and precipitation of kernicterus in new-borns.
So, vitamin K3 should not be used.
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